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Mutations in the periplasmic chaperone leading to loss of surface expression of the colonization factor CS6 in enterotoxigenic Escherichia coli (ETEC) clinical isolates.

Artikel i vetenskaplig tidskrift
Författare Matilda Nicklasson
Åsa Sjöling
Michael Lebens
Joshua Tobias
Anders Janzon
Lars Brive
Ann-Mari Svennerholm
Publicerad i Microbial Pathogenesis
Volym 44
Nummer/häfte 3
Sidor 246-54
ISSN 0882-4010
Publiceringsår 2008
Publicerad vid Institutionen för cell- och molekylärbiologi
Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Sidor 246-54
Språk en
Länkar dx.doi.org/10.1016/j.micpath.2007.0...
Ämnesord Enterotoxigenic Escherichia coli, Chaperone, Bacterial SNP, Adhesion, Virulence factor, Coli surface antigen 6 (CS6), Antigens, Bacterial, analysis, genetics, metabolism, Enterotoxigenic Escherichia coli, genetics, immunology, metabolism, Enterotoxins, Escherichia coli Infections, epidemiology, microbiology, Escherichia coli Proteins, analysis, genetics, metabolism, Molecular Chaperones, genetics, Mutation, genetics, Operon, Periplasmic Proteins, metabolism, Polymorphism, Single Nucleotide
Ämneskategorier Bioinformatik och systembiologi, Mikrobiologi inom det medicinska området

Sammanfattning

Enterotoxigenic Escherichia coli (ETEC) cause diarrhoea by adhesion to human enterocytes by one or more colonization factors (CFs) and secretion of heat-labile (LT) and/or heat-stable (ST) enterotoxins. Expression of coli surface antigen 6 (CS6) on the bacterial surface, usually associated with ETEC strains that produce ST alone or in combination with LT, is rarely found in strains expressing only LT. However, a number of LT-only strains which are genotypically positive but phenotypically negative for CS6 have been identified. In this study, eight such strains from India and Guinea-Bissau belonging to different clones were analysed. The CS6 operon cssABCD was transcribed but protein analyses suggested that the structural subunits CssA and CssB of CS6 were absent in the periplasm. Most strains contained truncating mutations within the periplasmic chaperone-encoding gene cssC and protein modelling indicated that this severely affected the substrate-binding capacity of the chaperone. A single-nucleotide polymorphism (SNP) (A-->T) in the 5'-untranslated region of cssC distinguished the eight strains from ETEC strains that do express CS6 on the surface and may be a potential marker for ETEC strains containing phenotypically silent cssABCD. The study emphasizes the importance of using both genotypic and phenotypic methods in epidemiological studies of ETEC, e.g. for vaccine development.

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